D. melanogaster development was markedly retarded and its survival decreased by larvae treatment with compounds being strong inducers of the cytochrome P‐450 2B in mammals— phenobarbital (PB*), perfluorodecaline (PFD), transstilbene oxide (TSO), and triphenyldioxane (TPD). At the same time, the weak inducer hexobarbital or the selective cytochrome P‐450 inducer in mice but not in rats 1,4‐bis[2‐(dichloropyridyl‐oxy)]‐benzene (DPB) did not affect the larvae development. The cytochrome P‐450 1A1 inducers benzo(a)anthracene (BA) and β‐naphtoflavone (BNF) were also not effective. The toxicity of phenobarbital was shown to be decreased by the cytochrome P‐450 inhibitor piperonyl butoxide by adding 20‐hydroxyecdysone or by treatment with aminophylline—the indirect enhancer of ecdysone production in the larval prothoracic gland. The hypothesis of the moulting hormone degradation as the cause of elevated larvae mortality resulting from the induced high mixed function oxidase activity has been discussed.
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